Vladimir Matchkov

Involvement of the Na + ,K +-ATPase isoforms in control of cerebral perfusion

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DOI

New Findings: What is the topic of this review? In this review, we consider the role of the Na + ,K + -ATPase in cerebrovascular function and how it might be changed in familial hemiplegic migraine type 2 (FHM2). The primary focus is involvement of the Na + ,K + -ATPase isoforms in regulation of cerebrovascular tone. What advances does it highlight? In this review, we discuss three overall distinct mechanisms whereby the Na + ,K + -ATPase might be capable of regulating cerebrovascular tone. Furthermore, we discuss how changes in the Na + ,K + -ATPase in cerebral arteries might affect brain perfusion and thereby be involved in the pathology of FHM2. Abstract: Familial hemiplegic migraine type 2 (FHM2) has been characterized by biphasic changes in cerebral blood flow during a migraine attack, with initial hypoperfusion followed by abnormal hyperperfusion of the affected hemisphere. We suggested that FHM2-associated loss-of-function mutation(s) in the Na + ,K + -ATPase α2 isoform might be responsible for these biphasic changes in several ways. We found that reduced expression of the α2 isoform leads to sensitization of the contractile machinery to [Ca 2+ ] i via Src kinase-dependent signal transduction. This change in sensitivity might be the underlying mechanism for both abnormally potentiated vasoconstriction and exaggerated vasorelaxation. Moreover, the functional significance of the Na + ,K + -ATPase α2 isoform in astrocytes provides for the possibility of elevated extracellular potassium signalling from astrocytic endfeet to the vascular wall in neurovascular coupling.

Original languageEnglish
JournalExperimental Physiology
Volume104
Issue7
Pages (from-to)1023-1028
Number of pages6
ISSN0958-0670
DOIs
Publication statusPublished - 2019

    Research areas

  • blood vessels, Na ,K -ATPase, neurovascular coupling

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